ArticleAmerican journal of respiratory and critical care medicine2013
Histone 3.3 participates in a self-sustaining cascade of apoptosis that contributes to the progression of chronic obstructive pulmonary disease.
Article in American journal of respiratory and critical care medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
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- Fantastic proteins and where to find them - histones, in the nucleus and beyond.Journal of cell science · 2024Review
- Multi-Omics Analysis Identified Drug Repurposing Targets for Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Article
- Decreased histone expression in chronic rhinosinusitis with nasal polyps.Asia Pacific allergy · 2024Article
- Distinct functional neutrophil phenotypes in sepsis patients correlate with disease severity.Frontiers in immunology · 2024Article
- Liquid Liver Biopsy for Disease Diagnosis and Prognosis.Journal of clinical and translational hepatology · 2023Review
- Extracellular Acetylated Histone 3.3 Induces Inflammation and Lung Tissue Damage.Biomolecules · 2023Article
- Incorporation of paclitaxel in mesenchymal stem cells using nanoengineering upregulates antioxidant response, CXCR4 expression and enhances tumor homing.Materials today. Bio · 2023Article
- Circulating Histones to Detect and Monitor the Progression of Cancer.International journal of molecular sciences · 2023Review
- Histone-stimulated platelet adhesion to mouse cremaster venules in vivo is dependent on von Willebrand factor.Microcirculation (New York, N.Y. : 1994) · 2022Article
- Extracellular histones aggravate autoimmune arthritis by lytic cell death.Frontiers in immunology · 2022Article
- HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons.Autophagy · 2021Article
- Eosinophil-mediated inflammation in the absence of eosinophilia.Asia Pacific allergy · 2021Review
- Article
- The impact of neutrophil extracellular trap from patients with systemic lupus erythematosus on the viability, CD11b expression and oxidative burst of healthy neutrophils.BMC immunology · 2021Article
- A looming role of mitochondrial calcium in dictating the lung epithelial integrity and pathophysiology of lung diseases.Mitochondrion · 2020Review
- Fibrinogen protects neutrophils from the cytotoxic effects of histones and delays neutrophil extracellular trap formation induced by ionomycin.Scientific reports · 2020Article
- Osteopontin protects against lung injury caused by extracellular histones.Mucosal immunology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleShifts in the gene expression of nuclear protein in chronic obstructive pulmonary disease (COPD), a progressive disease that is characterized by extensive lung inflammation and apoptosis, are common; however, the extent of the elevation of the core histones, which are the major components of nuclear proteins and their consequences in COPD, has not been characterized, which is important because extracellular histones are cytotoxic to endothelial and airway epithelial cells.
objectivesTo investigate the role of extracellular histones in COPD disease progression.
methodsWe analyzed the nuclear lung proteomes of ex-smokers with and without the disease. Further studies on the consequences of H3.3 were also performed. MEASUREMENTS AND MAIN
resultsA striking finding was a COPD-specific eightfold increase of hyperacetylated histone H3.3. The hyperacetylation renders H3.3 resistant to proteasomal degradation despite ubiquitination; when combined with the reduction in proteasome activity that is known for COPD, this resistance helps account for the increased levels of H3.3. Using anti-H3 antibodies, we found H3.3 in the airway lumen, alveolar fluid, and plasma of COPD samples. H3.3 was cytotoxic to lung structural cells via a mechanism that involves the perturbation of Ca(2+) homeostasis and mitochondrial toxicity. We used the primary human airway epithelial cells and found that the antibodies to either the C or N terminus of H3 could partially reverse H3.3 toxicity.
conclusionsOur data indicate that there is an uncontrolled positive feedback loop in which the damaged cells release acetylated H3.3, which causes more damage, adds H3.3 release, and contributes toward the disease progression.
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